Loss of immunoreactivity for glial fibrillary acidic protein (GFAP) in astrocytes as a marker for profound tissue damage in substantia nigra and basal cortical areas after status epilepticus induced by pilocarpine in rat.

Status epilepticus induced by pilocarpine in rats induces massive tissue damage comprising neurons and astrocytes (incomplete infarction) in substantia nigra pars reticulata (SNR) and in basal cortical areas (BCTX). Immunohistochemistry with a polyclonal antiserum and a monoclonal antibody to GFAP were used here to study the astroglial damage in these regions. Control sections showed a strong labeling for glial fibrillary acidic protein (GFAP) for both antibodies in SNR and BCTX. At 1 day after induction of seizures, labeling with the polyclonal antibodies showed diffuse increase within the lesioned areas and enhanced staining of astrocytes at the border zones. However, staining with the monoclonal antibody was abolished. At 3 days, labeling with both the polyclonal antiserum and the monoclonal antibody was severely reduced within the damaged regions. Reactive astrocytes in the surround of the infarct showed enhanced labeling with both antibodies. This combination of enhanced labeling with polyclonal antibodies and decreased labeling with the specific monoclonal antibody for GFAP can be taken as indicator for acute glial cell damage in seizures and related experimental conditions.